METHODS: A 2D model in the axisymmetric coordinates was developed to simulate the electro-thermophysiological responses of the tissue during a single probe bipolar RFA. Two different probe configurations were considered, namely the configuration where the active electrode is longer than the ground and the configuration where the ground electrode is longer than the active. The mathematical model was first verified with an existing experimental study found in the literature.
RESULTS: Results from the simulations showed that heating is confined only to the region around the shorter electrode, regardless of whether the shorter electrode is the active or the ground. Consequently, thermal coagulation also occurs in the region surrounding the shorter electrode. This opened up the possibility for a better customized treatment through the development of RF probes with adjustable electrode lengths.
CONCLUSIONS: The electrode length was found to play a significant role on the outcome of single probe bipolar RFA. In particular, the length of the shorter electrode becomes the limiting factor that influences the mechanics of single probe bipolar RFA. Results from this study can be used to further develop and optimize bipolar RFA as an effective and reliable cancer treatment technique.
MATERIALS AND METHODS: Atrial arrhythmogenesis was investigated in Langendorff-perfused young (3-4 month) and aged (>12 month), wild type (WT) and peroxisome proliferator activated receptor-γ coactivator-1β deficient (Pgc-1β-/-) murine hearts modeling age-dependent chronic mitochondrial dysfunction during regular pacing and programmed electrical stimulation (PES).
RESULTS AND DISCUSSION: The Pgc-1β-/- genotype was associated with a pro-arrhythmic phenotype progressing with age. Young and aged Pgc-1β-/- hearts showed compromised maximum action potential (AP) depolarization rates, (dV/dt)max, prolonged AP latencies reflecting slowed action potential (AP) conduction, similar effective refractory periods and baseline action potential durations (APD90) but shortened APD90 in APs in response to extrasystolic stimuli at short stimulation intervals. Electrical properties of APs triggering arrhythmia were similar in WT and Pgc-1β-/- hearts. Pgc-1β-/- hearts showed accelerated age-dependent fibrotic change relative to WT, with young Pgc-1β-/- hearts displaying similar fibrotic change as aged WT, and aged Pgc-1β-/- hearts the greatest fibrotic change. Mitochondrial deficits thus result in an arrhythmic substrate, through slowed AP conduction and altered repolarisation characteristics, arising from alterations in electrophysiological properties and accelerated structural change.